ArticleFrontiers in immunology2017
TWEAK/Fn14 Activation Participates in Ro52-Mediated Photosensitization in Cutaneous Lupus Erythematosus.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Update on the Etiology and Pathogenesis of Erythrodermic Psoriasis.Journal of inflammation research · 2026Review
- Research progress on TWEAK/Fn14 signaling in chronic wound healing.Frontiers in surgery · 2026Review
- Transforming growth factor alpha promotes bullous pemphigoid pathogenesis by disrupting cell adhesion and inducing inflammation.Cellular and molecular life sciences : CMLS · 2025Article
- Cutaneous Lupus Erythematosus: An Update on Pathogenesis and Future Therapeutic Directions.American journal of clinical dermatology · 2023Review
- IL-33/ST2 Activation Is involved in Ro60-Regulated Photosensitivity in Cutaneous Lupus Erythematosus.Mediators of inflammation · 2022Article
- An Overview of Neonatal Lupus with Anti-Ro Characteristics.International journal of molecular sciences · 2021Review
- An Update on the Pathogenesis of Cutaneous Lupus Erythematosus and Its Role in Clinical Practice.Current rheumatology reports · 2020Review
- Experimental atopic dermatitis is dependent on the TWEAK/Fn14 signaling pathway.Clinical and experimental immunology · 2020Article
- TWEAK Promotes the Proliferation of Squamous Cell Carcinoma Cells Through Activating cIAP1 Signals.Frontiers in oncology · 2020Article
- Fn14 Participates in Neuropathic Pain Through NF-κB Pathway in Primary Sensory Neurons.Molecular neurobiology · 2019Article
- Pentagalloylglucose Inhibits the Replication of Rabies Virus via Mediation of the miR-455/SOCS3/STAT3/IL-6 Pathway.Journal of virology · 2019Article
- Cutaneous lupus erythematosus: new insights into pathogenesis and therapeutic strategies.Nature reviews. Rheumatology · 2019Review
- Mechanistic insights into environmental and genetic risk factors for systemic lupus erythematosus.American journal of translational research · 2019Review
- Anti-double Stranded DNA Antibodies: Origin, Pathogenicity, and Targeted Therapies.Frontiers in immunology · 2019Review
- Tumor Necrosis Factor (TNF) Receptor Expression Determines Keratinocyte Fate upon Stimulation with TNF-Like Weak Inducer of Apoptosis.Mediators of inflammation · 2019Article
- Diagnostic Utility of Separate Anti-Ro60 and Anti-Ro52/TRIM21 Antibody Detection in Autoimmune Diseases.Frontiers in immunology · 2019Observational
- Fn14 deficiency ameliorates psoriasis-like skin disease in a murine model.Cell death & disease · 2018Article
- Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice.Frontiers in pharmacology · 2018Article
- Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice.Journal of immunology research · 2018Article
- Human and Murine Evidence for Mechanisms Driving Autoimmune Photosensitivity.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) binds to its sole receptor fibroblast growth factor-inducible 14 (Fn14), participating in various inflammatory responses. Recently, TWEAK/Fn14 activation was found prominent in the lesions of cutaneous lupus erythematosus (CLE). This study was designed to further reveal the potential role of this pathway in Ro52-mediated photosensitization. TWEAK, Fn14, and Ro52 were determined in the skin lesions of patients with CLE. Murine keratinocytes received ultraviolet B (UVB) irradiation or plus TWEAK stimulation and underwent detection for Ro52 and proinflammatory cytokines. The chemotaxis of J774.2 macrophages was evaluated on TWEAK stimulation of cocultured keratinocytes. We found that TWEAK, Fn14, and downstream cytokines were highly expressed in CLE lesions that overexpressed Ro52. Moreover, TWEAK enhanced the UVB-induced Ro52 upregulation in murine keratinocytes. Meanwhile, TWEAK stimulation of keratinocytes favored the migration of macrophages through promoting the production of chemokine C-C motif ligands 17 and 22. Furthermore, Fn14 siRNA transfection or nuclear factor-kappa B (NF-κB) inhibitor abrogated the TWEAK enhancement of Ro52 expression in keratinocytes. Similarly, TNF receptor associated factor 2 (TRAF2) siRNA reduced the protein level of Ro52 in these cells upon TWEAK stimulation. Interestingly, UVB irradiation increased the expression of TNF receptor type 1 (TNFR1) but not affecting TNFR2 expression in keratinocytes. In conclusion, the TWEAK/Fn14 signaling participates in Ro52-mediated photosensitization and involves the activation of NF-κB pathway as well as the function of the TRAF2/TNFR partners.
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